Citric acid, cis-aconitic acid, and isocitric acid are the first three metabolites in the Krebs Citric Acid energy production cycle, which operates in the mitochondria of your cells.
Citrate, cis-Aconitate (and Isocitrate) are involved in both energy production and removal of toxic ammonia.
High levels can indicate ammonia toxicity. Chronic loss of these valuable compounds can contribute to loss of organ reserve and disturbances in neurological function. If they are low they can indicate a need for essential amino acids, especially arginine.
DECREASED urinary citrate if:
Acidosis, acid loads
Diet
Medical disorders
Beta-oxidation disorders (liver)
Gastrointestinal disorders (diarrhea, malabsorption)
Chronic fatigue disorder
Kidney disease
Autosomal dominant polycystic kidney disease (ADPKD)
Decreased urinary citrate, beta-hydroxyisovalerate
Chronic renal failure
Decreased GFR
May decrease urinary citrate, cis-aconitate, homovanillate
Menopause
Medications:
Toxic exposure:
-------------------
LOW LEVELS of citrate may occur if there are nutritional enzyme inhibitions or inherited low-activity enzyme variants on the synthesis pathway, or if there are low levels of precursor (pyruvate) available. Low-calorie diets or problems with the precursor pathways may decrease citrate levels. Lower levels of citrate may also occur if there are problems with the liver’s fatty acid beta-oxidation pathway. Low levels of citrate have been associated with chronic fatigue syndrome. Urinary tract infections may decrease urinary citrate and increase lactate and succinate excretion.
If citrate levels are low, but pyruvate and lactate levels are higher, there may be an inherited low-activity enzyme of the rate-limiting enzyme citrate synthase or inhibition due to
toxic exposures.
Arsenic or other toxic metals may prevent the conversion of pyruvate into citrate. Arsenic may be found in well water, in factory-farmed poultry, alcoholic beverages and as a pesticide contaminant in conventionally-farmed fruits and vegetables. Arsenic exposure can increase alpha-ketoglutarate and pyruvate, while citrate, succinate, and pyroglutamate levels decrease.
Inherited low-activity citrate synthase variants may require more dietary citrate (lemonade, citrus fruits, etc.).
The beta-oxidation pathway in the liver is the primary fatty acid breakdown pathway. Inhibition of the pathway can increase adipate and suberate, and may also increase ethylmalonate and ethylsuccinate levels.
Chronic fatigue may increase pyruvate and decrease citrate, cis-aconitate, isocitrate, malate.
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Elevated urinary citrate levels when:
Diet:
High carbohydrate intake
High citrate/citrus intake
High (4-5 servings/day) dairy intake
May decrease hippurate
High-dose vitamin D
Endocrine disorders:
High estrogen levels (birth control or estrogen replacement therapies)
Parathyroid extract or hyperparathyroidism
Renal function:
Renal tubular reabsorption defects
Alkalosis, dietary alkali loads
Hypercalcuria
Toxic exposures:
---------------------
HIGH LEVELS of citrate may occur when there are nutritional enzyme inhibitions of the breakdown pathways, inherited low-activity enzymes are present, if there are high levels of its precursor (pyruvate, malate) or if there are higher levels of its downstream products (cis-aconitate). High levels of citrate may be damaging, and can increase oxidative stress, nitric oxide (nitrosative stress), and pro-inflammatory prostaglandins. Endocrine or kidney disorders may increase citrate levels, as may dietary citrate intakes (citrus, dairy) or highly alkaline diets. Toxic metals such as lead may also increase levels.
Citrate levels may also increase if citrate cannot be broken down outside the mitochondria in the cytoplasm. This cellular breakdown may be supported with magnesium and the use of a plant-based, low-fat diet.
Lead exposure increases oxidative stress and can inhibit aconitase. Lead can leach out of bones during and after andropause or menopause. Lead solder was not banned in housing construction until about 1990 and may still be found in drinking water.
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2-Decenedioic Acid, 2-ET-3-OH-Propionic, 2-Hydroxyadipic, 2-Hydroxybutyric, 2-Hydroxyglutaric, 2-Hydroxyisocaproic, 2-Hydroxyisovaleric, 2-Methyl, 3-Hydroxybutyric, 2-Methylacetoacetic, 2-Methylbutrylglycine, 2-Methylglutaconic Acid, 2-Octenedioic acid, 2-Octenoic Acid, 2-OH-3ME-Valeric, 2-Oxo-3-methylvaleric, 2-OXO-Butyric Acid, 2-OXOADIPIC, 2-Oxoglutaric, 2-Oxoisocaproic, 2-Oxoisovaleric, 2OH-Phenylacetic Acid, 3-Hydroxyadipic, 3-Hydroxybutyric, 3-Hydroxyglutaric, 3-Hydroxyisobutyric, 3-Hydroxyisovaleric, 3-Hydroxypropionic, 3-Hydroxysebacic, 3-Hydroxyvaleric, 3-Methylcrotonylglycine, 3-Methylglutaconic, 3-Methylglutaric, 3-OH-3-Methylglutaric, 30H-ISOVALERIC ACID, 3OH-2-Methylvaleric Acid, 3OH-Dodecanedioic Acid, 3OH-Dodecanoic Acid, 4 HYDROXYCYCLOHEX- ANEACETIC, 4-Hydroxphenyllactic, 4-Hydroxybutyric, 4-Hydroxyphenylacetic, 4-Hydroxyphenylpyruvic, 4OH-Phenylpropionic Acid, 5-HIAA, 5-Oxoproline, 5OH-Hexanoic Acid, Acetoacetic, Aconitic, Ur, Adipic, Butyrylglycine, Citric, Crotonylglycine, Decadienedioic, Dodecanedioic, Ethylmalonic, Fumaric, Glutaconic, Glutaric, Glyceric Acid, Hexanoylglycine, Homogentisic, HOMOVANILLIC ACID, Isobutyrylglycine, Isocitric, Isovaleryglycine, Lactic, Lactic Acid, Malic, Malonic, Methylcitric, Methylmalonic, Methylsuccinic, Mevalonolactone, N ACETYLASPARTIC, N-AcetylTyrosine, N-Valerylglycine, Octanoic, Orotic, Phenylacetic, Phenyllactic, Phenylpropionylglycine, Phenylpyruvic, Propionylglycine, Pyruvic, Sebacic, Suberic, Suberylglycine, Succinic, Succinylacetone, Thymine, Tiglylglycine, Trans-Cinnamoylglycine, Uracil, VMA